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rakesh7biswas
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« on: May 12, 2006, 01:13:50 AM »

hi sir,
 
this morning i saw a multiple sclerosis patient,24 years old, female. she also have thyrotoxicosis and recently neutropenic sepsis. she came 1 montah back with complain of infected bedsores and diminision of vision..
 
on examination..
on the upper limb she has hypotonia but with hyperreflexia. muscle power is about 4-5.
on lower limb examination, wasting are seen at the thigh mostly on the right side, and also we could see involuntary jerky movement of dorsiflexion and flexion of the knee joint.
tones and reflexes are increase bilaterally, clonus are seen at the patellar, but not in the plantar region. muscle power on the lower limb could not be assessed because of the jerky movement but i think its about 3-4, lesser on the right side.
when we do finger nose test xmnination on her, there was overshooting, seen bilaterally, but when she did dysdidokokinesia it appear to be normal.
 
but this afternoon when we tried to demonstrate clonus to the other batch, it is not there..
can u explain it sir.   
 
thank you sir..


I think you are talking about the same patient further details of whom I paste below with also a possible solution to your predicament at the end:
Her problems started with visual loss (due to optic neuritis) 9 years back. 2 months later she developed sudden weakness (focal neuro deficit) in her left upper and lower limbs that gradually improved in 4 weeks. 8 months later she had a similar weakness in her right side lasted for 3 months. She has been having multiple such remissions and relapses of weakness since then. In december 2005 patient had her last major attack following which she is generally bed bound due to qudri/paraparesis. If you examine her you shall find hypertonia in her both lower limbs with exaggerated reflexes along with an extensor planter suggestive of upper motor neuron lesion (at the spinal cord-- exact segmental level needs to be determined by a recent examination but the last we examined her the power was reduced even in the upper limbs suggestive of a lesion in cervical spinal cord). Clinically it has been thought to be multiple sclerosis because of the relapsing and remitting course which is a hallmark of this disease along with multiple long tract lesions demonstrable clinically (optic nerve and pyramidal tract invlovement). Just check if she has had an MRI done which is needed to confirm the lesions of multiple sclerosis. The 10 batch group posted in medicine saw this case right on the very day I had taken the lecture class on Multiple sclerosis for them. 
 
Yes I remember the findings are very much the same as you describe (when I had seen her 2 months back). Reflexes can fade temporarily (and cause embarrassment to the demonstrator as perhaps happened to you). If you try again after some rest it will come back. Rakesh

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rakesh7biswas
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« Reply #1 on: May 12, 2006, 01:19:32 AM »

2;
 
we went to see the patient of multiple sclerosis.on eye examination,visual acuity was 4 foot away for both eyes as she has blurred vision.

she was having upper limbs hypotonia,muscle power grade 4/5 of both sides and normal reflexes.meanwhile her lower limbs were hyperreflexia(it bends even when we tried to take off her socks) and hypertonia.patellar and ankle clonus are present on both sides,while babinskis sign were positive too.her bed sore has almost healed.there were cerebellar signs elicited like shooting of finger nose test.dysdiadochokinesia was not seen and knee heel test cant be performed as she has hyperreflexia of both lower limbs.

Response -The dysdiadochokinesia may be false positive as one needs to have normal power to test for co-ordination. She looks more moribund than the last month with her cachexia and alopecia. Possibly it’s because of the immunosuppresants that she is receiving. Do find out what drugs she is recieving and what are the other side effects they are producing (on her blood count, biochemical parameters etc). She is one of the cases for the chronic paralysis research group. Find out the evidence base regarding the efficacy of the immunosuppresants she is receiving in terms of treatment outcome for the disease (the cause of her chronic paralysis). Like tolerating all these side effects that you can see on the general survey would still be worthwhile if her neurodeficits improved. We also need to follow her up closely for this so don’t forget to take her phone number and complete address. Also take informed consent from all the patients (as it would be necessary for putting all this online even if anonymity is maintained—translate the informed consent form into Malay).

Rakesh
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